Year-end Sale % OFF 
Abstract
Autoimmune rheumatic diseases (ARDs), affecting ~1–1.5% of all humans, are associated with considerable life long morbidity and early mortality. Early studies in the 1990s showed numerical changes of the recently discovered γδ T cells in the peripheral blood and in affected tissues of patients with a variety of ARDs, kindling interest in their role in the immuno-pathogenesis of these chronic inflammatory conditions. Indeed, later studies applied rapid developments in the understanding of γδ T cell biology, including antigens recognized by γδ T cells, their developmental programs, states of activation, and cytokine production profiles, to analyze their contribution to the pathological immune response in these disorders. Here we review the published studies addressing the role of γδ T in the major autoimmune rheumatic diseases, including rheumatoid arthritis, juvenile idiopathic arthritis, ankylosing spondylitis, systemic lupus erythematosus and scleroderma, and animal models thereof. Due to their unique properties spanning adaptive and innate immune functions, the ever deeper understanding of this unique T cell population is shedding new light on the pathogenesis of, while potentially enabling new therapeutic approaches to, these diseases.
Highlights
In the mid 1980s, the previously elusive nature of the T cell receptor (TCR) expressed by CD4+and CD8+ major histocompatibility complex (MHC) restricted T cells had just been established to be encoded by rearranging α and β TCR gene [1,2]
We summarize research from publications found in PubMed in which the major autoimmune rheumatic disorders (ARDs) (rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), systemic lupus erythematosus (SLE), ankylosing spondylitis (AS) and systemic sclerosis (SSc)) were addressed with reference to γδ T cells
The lead authors of the first papers to describe γδ TCR and γδ T cells were both rheumatologists, a profession which focuses on Autoimmune rheumatic diseases (ARDs) [4,5]
Summary
In the mid 1980s, the previously elusive nature of the T cell receptor (TCR) expressed by CD4+. The serendipitous discovery of a third rearranging gene, termed γ, in a murine clone of cytotoxic αβ T cells, confounded by absent expression of a protein encoded by this gene, raised questions relating to the role of this newcomer [3] These were resolved in 1986, when two papers revealed human thymocyte derived CD4− CD8− T cell clones and peripheral blood T cell clones expressing a second TCR composed of two polypeptide chains associated with the CD3 molecule, one of which was encoded by the “mysterious” γ gene, and the second later shown to be encoded by a fourth TCR gene, δ [4,5,6]. For example, imprinting of subsets of γδ T cells resulting in an innate ability to produce the potent proinflammatory interleukin (IL)-17, in the absence of TCR activation, takes place during thymic maturation [13] This contrasts with the requirement for antigenic encounters in peripheral lymph nodes, in order for conventional naïve αβ T cells to acquire effector functions. Given the increasing understanding of the underlying principles governing γδ T cell recognition and physiology, these and future studies are contributing to a wider comprehension of the pathogenesis of ARDs, and may point to new ways of treating these devastating conditions
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
